Aims
Adiponectin (APN) is an adipocyte-derived bioactive molecule with anti-diabetic and anti-atherogenic properties. Although the anti-diabetic effects of APN are mediated by AdipoR1 and AdipoR2, the anti-atherogenic mechanisms of APN remain unclear. The aim of this study was to determine the serum molecule inhibiting APN functions.
Background and aims
Adiponectin (APN) is an adipocyte-derived bioactive molecule with anti-diabetic and anti-atherogenic properties. Although the anti-diabetic effects of APN are mediated by AdipoR1 and AdipoR2, the anti-atherogenic mechanisms of APN remain unclear. The aim of this study was to determine the serum molecule inhibiting APN functions.
Conclusions
The increment of serum M2BP-APN complex could be a novel risk factor for CAD, through the abolishment of the anti-atherogenic effects of APN.
Results
By immunoprecipitation with an anti-APN antibody and mass spectrometry, we identified Mac-2 binding protein (M2BP) as a novel serum APN-binding protein. The association of M2BP and APN was confirmed using reconstituted proteins in vitro. Serum M2BP-APN complex levels were markedly higher in male patients with coronary artery disease (CAD) than in healthy subjects. M2BP abrogated the suppressive effects of APN on tumour necrosis factor (TNF)-α-induced inflammation in vascular endothelial cells. Conclusions: The increment of serum M2BP-APN complex could be a novel risk factor for CAD, through the abolishment of the anti-atherogenic effects of APN.